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Chapter 58 Poisonings

Of the more than 2 million human poisoning exposures reported annually to the National Poison Data Systems of the American Association of Poison Control Centers (AAPCC), more than 50% occur in children <6 yr old. Almost all of these exposures are unintentional and reflect the propensity for young children to put virtually anything in their mouths.

More than 90% of toxic exposures in children occur in the home, and most involve only a single substance. Ingestion accounts for the vast majority of exposures, with a minority occurring via the dermal, inhalational, and ophthalmic routes. Approximately 50% of cases involve nondrug substances, such as cosmetics, personal care items, cleaning solutions, plants, and foreign bodies. Pharmaceutical preparations account for the remainder of exposures, and analgesics, topical preparations, cough and cold products, and vitamins are the most commonly reported categories.

More than 85% of poisoning exposures in children <6 yr can be managed without direct medical intervention, either because the product involved is not inherently toxic or the quantity of the material involved is not sufficient to produce clinically relevant toxic effects (Table 58-1). However, a number of substances are potentially highly toxic to toddlers in small doses (Table 58-2). Fatalities often result from carbon monoxide, iron, analgesics, hydrocarbons, cardiovascular drugs, antidepressants, and pesticides. Although the majority of exposures occur in children <6 yr, only 2.8% of the reported deaths occur in this age group. In addition to the exploratory nature of ingestions in young children, product safety measures, poison prevention education, early recognition of exposures, and around-the-clock access to regionally based poison control centers all contribute to the favorable outcomes in this age group.


* The potential for toxicity depends on the magnitude and amount of exposure. These agents are considered nontoxic or minimally toxic for mild to moderate exposure. The potential for toxicity increases with increased amount of exposure.


Antimalarials (chloroquine, quinine) Seizures, cardiac arrhythmias
Benzocaine Methemoglobinemia
β-Blockers (lipid-soluble β-blockers [e.g., propranolol] are more toxic than water-soluble β-blockers [e.g., atenolol]) Bradycardia, hypotension, hypoglycemia
Calcium channel blockers Bradycardia, hypotension, hyperglycemia
Camphor Seizures
Clonidine Lethargy, bradycardia, hypotension
Diphenoxylate and atropine (Lomotil) CNS depression, respiratory depression
Hypoglycemics, oral (sulfonylureas and meglitinides) Hypoglycemia, seizures
Lindane Seizures
Monoamine oxidase Inhibitors Hypertension followed by delayed cardiovascular collapse
Methyl salicylates Tachypnea, metabolic acidosis, seizures
Opioids (especially methadone, lomotil and suboxone) CNS depression, respiratory depression
Phenothiazines (chlorpromazine, hioridazine) Seizures, cardiac arrhythmias
Theophylline Seizures, cardiac arrhythmias
Tricyclic antidepressants CNS depression, seizures, cardiac arrhythmias, hypotension

CNS, central nervous system.

* “Small dose” typically implies 1 or 2 pills or 5 mL.

Poison prevention education should be an integral part of all well child visits, starting at the 6-mo visit. Counseling parents and other caregivers about potential poisoning risks, how to poison-proof a child’s environment, and what to do if an ingestion or exposure occurs diminishes the likelihood of serious morbidity or mortality. Poison prevention education materials are available from the American Academy of Pediatrics and regional poison control centers. A network of poison control centers exists in the U.S., and anyone at any time can contact a regional poison center by calling a toll-free number: 1-800-222-1222. Parents should be encouraged to share this number with grandparents, relatives, and any other caregivers.

Poisoning exposures in children 6-12 yr old are much less common, involving only ~ 6% of all reported pediatric exposures. A second peak in pediatric exposures occurs in adolescence. Exposures in the adolescent age group are primarily intentional (suicide or abuse or misuse of substances) and thus often result in more severe toxicity (see Chapter 108). Families should be informed and given anticipatory guidance that over-the-counter (OTC) and prescription medications and even household products (e.g., inhalants) are common sources of adolescent exposures. Adolescents (ages 13-19 yr) accounted for 56 of the 102 reported poison-related pediatric deaths in 2007. Pediatricians should be aware of the signs of drug abuse or suicidal ideation in this population and should aggressively intervene (Chapter 108).

Approach to the Poisoned Patient

The initial approach to the patient with a witnessed or suspected poisoning should be no different than that in any other sick child, starting with stabilization and rapid assessment of the airway, breathing, circulation, and mental status (Chapter 62). A serum dextrose concentration should be obtained early in the evaluation of any patient with altered mental status. A targeted history and physical examination serves as the foundation for a thoughtful differential diagnosis, which can then be further refined through laboratory testing and other diagnostic studies.

Initial Evaluation


Obtaining an accurate problem-oriented history is of paramount importance. Intentional poisonings (suicide attempts; abuse or misuse) are typically more severe than unintentional, exploratory ingestions. In patients without a witnessed exposure, historical features such as age of the child (toddler or adolescent), acute onset of symptoms without prodrome, sudden alteration of mental status, multiple system organ dysfunction, or highs levels of household stress should suggest a possible diagnosis of poisoning.

Description of the Exposure

For household and workplace products, names (brand, generic, chemical) and specific ingredients, along with their concentrations, can often be obtained from the labels. Poison control center specialists can also help to identify possible ingredients and review the potential toxicities of each component. In cases of suspected ingestion, poison center specialists can help identify pills based on markings, shape, and color. If referred to the hospital for evaluation, parents should be instructed to bring the products, pills, and/or containers with them to assist with identifying and quantifying the exposure. If a child is found with an unknown pill in his or her mouth, the history must include a list of all medications in the child’s environment (including medications that grandparents, caregivers, or other visitors might have brought into the house). In the case of an unknown exposure, clarifying where the child was found (e.g., garage, kitchen, laundry room, bathroom, backyard, workplace) can help to generate a list of potential toxins.

Next, it is important to clarify the timing of the ingestion and to obtain some estimate of how much of the substance was ingested. In general, it is better to overestimate the amount ingested in order to prepare for the worst-case scenario. Counting pills or measuring the remaining volume of a liquid ingested can sometimes be useful in generating estimates.

For inhalational, ocular, or dermal exposures, the concentration of the agent and the length of contact time with the material should be determined as well as possible.


Obtaining a description of symptoms experienced after ingestion, including their timing of onset relative to the time of ingestion and their progression, can help to generate a list of potential toxins and to predict the severity of the ingestion. Coupled with physical exam findings, reported symptoms assist practitioners in identifying toxidromes or recognized poisoning syndromes suggestive of poisoning from specific substances or classes of substances (Tables 58-3 and 58-4).


Bitter almonds Cyanide
Acetone Isopropyl alcohol, methanol, paraldehyde, salicylates
Alcohol Ethanol
Wintergreen Methyl salicylate
Garlic Arsenic, thallium, organophosphates, selenium
Miosis Opioids (except propoxyphene, meperidine, and pentazocine), organophosphates and other cholinergics, clonidine, phenothiazines, sedative-hypnotics, olanzapine
Mydriasis Atropine, cocaine, amphetamines, antihistamines, TCAs, carbamazepine, serotonin syndrome, PCP, LSD, post-anoxic encephalopathy
Nystagmus Phenytoin, barbiturates, sedative-hypnotics, alcohols, carbamazepine, PCP, ketamine, dextromethorphan
Lacrimation Organophosphates, irritant gas or vapors
Retinal hyperemia Methanol
Diaphoresis Organophosphates, salicylates, cocaine and other sympathomimetics, serotonin syndrome, withdrawal syndromes
Alopecia Thallium, arsenic
Erythema Boric acid, elemental mercury, cyanide, carbon monoxide, disulfuram, scombroid, anticholinergics
Cyanosis (unresponsive to oxygen) Methemoglobinemia (e.g., benzocaine, dapsone, nitrites, phenazopyridine), amiodarone, silver
Salivation Organophosphates, salicylates, corrosives, ketamine, PCP, strychnine
Oral Burns Corrosives, oxalate-containing plants
Gum lines Lead, mercury, arsenic, bismuth
Diarrhea Antimicrobials, arsenic, iron, boric acid, cholinergics, colchicine, withdrawal
Hematemesis Arsenic, iron, caustics, NSAIDs, salicylates
Tachycardia Sympathomimetics (e.g., amphetamines, cocaine), anticholinergics, antidepressants, theophylline, caffeine, antipsychotics, atropine, salicylates, cellular asphyxiants (cyanide, carbon monoxide, hydrogen sulfide), withdrawal
Bradycardia β-Blockers, calcium channel blockers, digoxin, clonidine and other central α2 agonists, organophosphates, opioids, sedative-hypnotics
Hypertension Sympathomimetics (amphetamines, cocaine, LSD), anticholinergics, clonidine (early), monoamine oxidase inhibitors
Hypotension β blockers, calcium channel blockers, cyclic antidepressants, iron, phenothiazines, barbiturates, clonidine, theophylline, opioids, arsenic, amatoxin mushrooms, cellular asphyxiants (cyanide, carbon monoxide, hydrogen sulfide), snake envenomation
Depressed respirations Opioids, sedative-hypnotics, alcohol, clonidine, barbiturates
Tachypnea Salicylates, amphetamines, caffeine, metabolic acidosis (ethylene glycol, methanol, cyanide), carbon monoxide, hydrocarbons
Ataxia Alcohol, anticonvulsants, benzodiazepines, barbiturates, lithium, dextromethorphan, carbon monoxide, inhalants
Coma Opioids, sedative-hypnotics, anticonvulsants, cyclic antidepressants, antipsychotics, ethanol, anticholinergics, clonidine, GHB, alcohols, salicylates, barbiturates
Seizures Sympathomimetics, anticholinergics, antidepressants (especially TCAs, bupropion, venlafaxine), isoniazid, camphor, lindane, salicylates, lead, organophosphates, carbamazepine, tramadol, lithium, ginkgo seeds, water hemlock, withdrawal
Delirium/psychosis Sympathomimetics, anticholinergics, LSD, PCP, hallucinogens, lithium, dextromethorphan, steroids, withdrawal
Peripheral neuropathy Lead, arsenic, mercury, organophosphates

PCP, phencyclidine; LSD, lysergic acid diethylamide; TCA, tricylic antidepressants; NSAID, nonsteroidal anti-inflammatory drug; GHB, gamma hydroxybutyrate.

Laboratory Evaluation

For select intoxications (salicylates, some anticonvulsants, acetaminophen, iron, digoxin, methanol, lithium, theophylline, ethylene glycol, carbon monoxide), quantitative blood concentrations are integral to confirming the diagnosis and formulating a treatment plan. For most exposures, qualitative measurement is not possible and is not likely to alter management. Comprehensive, qualitative drug screens vary widely in their ability to detect toxins and generally add little information to the clinical assessment, particularly if the agent is known and the patient’s symptoms are consistent with that agent. If a drug screen is ordered, it is important to examine both serum and urine and to know that the components screened for in a toxicology screen, and the lower limits of detection, vary from hospital to hospital. In addition, the interpretation of most drug screens is hampered by false-positive and false-negative results. Most standard urine opiate screens won’t be positive after ingestion of a synthetic opioid (e.g., methadone, suboxone). Although the presence of some drugs (e.g., marijuana) might not be clinically useful, it can identify use of “gateway drugs” and an adolescent at risk for substance abuse. Consultation with a medical toxicologist can be helpful in interpreting drug screens and ordering specific drug levels or metabolites that can aid in patient management.

Toxicology screens may be indicated in the assessment of the neglected or allegedly abused child, because a positive toxicology screen can add substantial weight to a claim of abuse or neglect. In these cases and any case with medicolegal implications, any positive screen must be confirmed with gas chromatography/mass spectroscopy (GC/MS), which is considered the gold standard measurement for legal purposes.

Acetaminophen is a widely available medication and a commonly detected co-ingestant with the potential for severe toxicity. Given that patients might initially be asymptomatic and might not report acetaminophen as a co-ingestant, an acetaminophen level should be checked in all patients who present after an intentional exposure or ingestion. Furthermore, in any clinical situation with potential medicolegal implications, any positive drug screen should be confirmed by a more sensitive and specific method (typically GC/MS).

Based on the clinical presentation, additional labs tests that may be helpful include electrolytes and renal function (an elevated anion gap suggests a number of ingestions), serum osmolarity (toxic alcohols), complete blood count, liver function tests, urinalysis (crystals), co-oximetry, and a serum creatine kinase level (Table 58-5).

Additional Diagnostic Testing

An electrocardiogram (ECG) is a quick and noninvasive bedside test that can yield important clues to diagnosis and prognosis. Toxicologists pay particular attention to the ECG intervals (Table 58-6). A widened QRS interval suggests blockade of fast sodium channels, as may be seen after ingestion of tricyclic antidepressants, diphenhydramine, cocaine, propoxyphene, and carbamazepine, among others. A widened QTc interval suggests effects at the potassium rectifier channels and portends a risk of torsades de pointes.

Chest x-ray may reveal signs of pneumonitis (e.g., hydrocarbon ingestion), pulmonary edema (e.g., salicylate toxicity), or a foreign body. Abdominal x-ray can suggest the presence of a bezoar, demonstrate radiopaque tablets, or reveal drug packets in a body packer. Endoscopy may be useful after significant caustic ingestions. Further diagnostic testing is based on the differential diagnosis and pattern of presentation (Table 58-7).

Principles of Management

The four principles of management of the poisoned patient are decontamination, enhanced elimination, antidotes, and supportive care. Few patients meet criteria for all of these interventions, though clinicians should consider each option in every poisoned patient so as not to miss a potentially lifesaving therapy. Antidotes are available for relatively few poisons (Table 58-8), thus emphasizing the importance of meticulous supportive care and close clinical monitoring.

Poison control centers are staffed by nurses, pharmacists, and physicians specifically trained to provide expertise in the management of poisoning exposures. Parents should be instructed to call the poison control center (1-800-222-1222) for any concerning exposure. Poison specialists can assist parents in assessing the potential toxicity and severity of the exposure. In doing so, they can further determine which children can be monitored at home versus who should be referred to the emergency department (ED) for further evaluation and care. The American Academy of Clinical Toxicology has generated consensus statements for out-of-hospital management of common ingestions (e.g., acetaminophen, iron, selective serotonin reuptake inhibitors) that serve to guide poison center recommendations.


The majority of poisonings in children are due to ingestion, though exposures can also occur via inhalational, dermal and ocular routes. The goal of decontamination is to prevent absorption of the toxic substance. The specific method employed depends on the properties of the toxin itself and the route of exposure. Regardless of the decontamination method used, the efficacy of the intervention decreases with increasing time since exposure. Thus, decontamination should not be routinely employed for every poisoned patient. Instead, careful decisions regarding the utility of decontamination should be made for each patient and should include consideration of the toxicity and pharmacologic properties of the exposure, the route of the exposure, the time since the exposure, and the risks versus the benefits of the decontamination method.

Dermal and ocular decontamination begin with removal of any contaminated clothing and particulate matter, followed by flushing of the affected area with tepid water or normal saline. Treating clinicians should wear proper protective gear when performing irrigation. Flushing for a minimum of 10 to 20 minutes is recommended for most exposures, although some chemicals (e.g., alkaline corrosives) require much longer periods of flushing. Dermal decontamination, especially after exposure to adherent or lipophilic (e.g., organophosphates) agents, should include thorough cleansing with soap and water. Water should not be used for decontamination after exposure to highly reactive agents, such as elemental sodium, phosphorus, calcium oxide, and titanium tetrachloride. After an inhalational exposure, decontamination involves moving the patient to fresh air and administering supplemental oxygen if indicated.

Gastrointestinal (GI) decontamination is a controversial topic among medical toxicologists, with numerous studies documenting marked variability in recommendations. In general, GI decontamination strategies are most likely to be effective in the first hour after an acute ingestion. GI absorption may be delayed after ingestion of agents that slow GI motility (anticholinergic medications, opioids), massive pill ingestions, sustained-release preparations, and ingestions of agents that can form pharmacologic bezoars (e.g., enteric-coated salicylates). Thus, GI decontamination at >1 hr after ingestion may be considered in patients who ingest toxic substances with these properties. Described methods of GI decontamination include induced emesis with ipecac, gastric lavage, cathartics, activated charcoal, and whole-bowel irrigation (WBI). Of these, only activated charcoal and WBI are likely to have significant clinical benefit in management of the poisoned patient.

Syrup of Ipecac

Syrup of ipecac contains 2 emetic alkaloids that work in both the central nervous system (CNS) and locally in the GI tract to produce vomiting. In the 1960s, the American Academy of Pediatrics (AAP) lobbied for OTC availability of ipecac and in the 1980s recommended that ipecac be given to parents at the 6-month well child check, coupled with a discussion about poison prevention strategies. Since that time, studies have failed to document a significant clinical impact from the use of ipecac and have documented multiple adverse events from its use. Ipecac-induced emesis is especially contraindicated after the ingestion of caustics (acids and bases), hydrocarbons, and agents likely to cause rapid onset of CNS or cardiovascular symptoms. Ipecac abuse and cardiac toxicity is described in some adolescents with bulimia, and syrup of ipecac has been used in reported cases of factitious disorder by proxy.

After a review of the evidence and assessment of the risks and benefits of ipecac use, the American Academy of Pediatrics no longer recommends the use of syrup of ipecac. The 2004 American Academy of Clinical Toxicology (AACT)/European Association of Poison Control Centers and Clinical Toxicology (EAPCCT) position paper suggests that the use of ipecac in the ED be abandoned. A further review by the American Association of Poison Control Centers in 2005 suggests that out-of-hospital ipecac use only be considered in consultation with a medical toxicologist or poison control center if all of the following characteristics are met:

Single-Dose Activated Charcoal

Of all the described modalities of gastric decontamination, activated charcoal is thought to potentially be the most useful, though clinical data to support this claim is somewhat limited. Charcoal is “activated” via heating to extreme temperatures, creating an extensive network of pores that provides a very large adsorptive surface area. Many, but not all, toxins are adsorbed onto its surface, thus preventing absorption from the GI tract. Charcoal is most likely to be effective when given within 1 hr of ingestion. Some toxins, including heavy metals, iron, lithium, hydrocarbons, cyanide, and low-molecular-weight alcohols, are not significantly bound to charcoal (Table 58-9). Charcoal administration should also be avoided after ingestion of a caustic substance, because the presence of charcoal can impede subsequent endoscopic evaluation.

The dose of activated charcoal is 1 g/kg in children or 50-100 g in adolescents and adults. Before administering charcoal, one must ensure that the patient’s airway is intact or protected and that he or she has a benign abdominal exam. Approximately 20% of children vomit after receiving a dose of charcoal, emphasizing the importance of an intact airway and avoiding administration of charcoal after ingestion of substances that are particularly toxic when aspirated (e.g., hydrocarbons). If charcoal is given through a gastric tube, placement of the tube should be carefully confirmed before activated charcoal is given because instillation of charcoal directly into the lungs has disastrous effects. Constipation is another common side effect of activated charcoal, and in extreme cases, bowel perforation has been reported.

In young children, practitioners may attempt to improve palatability by adding flavorings (chocolate or cherry syrup) or giving the mixture over ice cream. Cathartics (sorbitol, magnesium sulfate, magnesium citrate) have been used in conjunction with activated charcoal to prevent constipation and accelerate evacuation of the charcoal-toxin complex. There is no evidence demonstrating their value and there are numerous reports of adverse effects from cathartics. Cathartics should be used with care in young children and should never be used in multiple doses because of the risk of dehydration and electrolyte imbalance.

Enhanced Elimination

Enhancing excretion is only useful for a few toxins; in these cases, enhancing elimination is a potentially lifesaving intervention (e.g., hemodialysis for methanol toxicity).


Antidotes are available for relatively few toxins (Table 58-11, and see Table 58-8), but early and appropriate use of an antidote is a key element in managing the poisoned patient. Consensus guidelines indicate the important antidotes to stock in facilities that provide emergency care.


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